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  • br Discussion Debate persists about how to best define


    Discussion Debate persists about how to best define the ER ECG pattern. There is consensus regarding definition of the malignant form of ER as a J-point elevation that could be (or not) associated with ST elevation [1]. In this case, a clear J-point elevation was seen, particularly in lead III (Fig. 2). The incidence of an ER pattern on surface ECG is reportedly up to 13%, and is higher in more recent studies [2–5]. It is more common in physically active young males and athletes [3]. Transient changes in the presence of J-point elevation poses a higher risk for VF [4], and J-point elevation amplitude has been associated with an elevated risk of these life-threatening arrhythmias [5]. The clinical presentation of ER syndrome is often unexpected malignant arrhythmias at first presentation [4]. In this case, the clinical VT/VF episode (Fig. 1) was initiated by closely coupled ventricular premature beats as previously described [2]. Acute suppression of the premature beat can be achieved with isoproterenol with oral quinidine for long-term control [5]. Catheter ablation has also been successfully performed [5].
    Conflict of interest
    Introduction A pak1 is a common medical device that provides electrical impulses, through electrodes, to the heart. The first device was implanted in 1958 [1], and there have been many important developments in the field since that time. Clinicians are confronted by various pacemaker malfunctions that are associated with these developments. We report a case of inappropriate pacing spikes, caused by atrial lead dislocation and subsequent engagement of the safety mode.
    Case report A 74-year-old female patient with a dual-chamber pacemaker (DDDR Pacemaker, Medtronic, Minneapolis, MN, USA) and tined lead electrodes (Medtronic, Minneapolis, MN, USA), which had been implanted 2 years previously, was admitted to the cardiology clinic with dyspnea. Physical examination was unremarkable, while electrocardiography (ECG) revealed dyssynchronization of the atrial and ventricular beats, with pacemaker spikes at the beginning and end of the QRS waves (Fig. 1A). Device interrogation revealed that the pacemaker was set to DDDR-mode, pak1 atrial and ventricular amplitude was 5.0V, pulse width was 0.5ms, and the atrial sensitivity had been set at 0.25mV at presentation. The atrial pacing threshold and ventricular pacing threshold were 1.0V and 0.5V, respectively. The patient was pacemaker-dependent. According to surface ECG and intracardiac ECG, atrial sensing was absent, although P waves were observed on the surface electrocardiogram. When atrial spikes occurred, the capture was ventricular, not atrial. After ventricular capture, there was an inappropriate spike at the end of the QRS wave (Fig. 2A). Therefore, atrial sensitivity was reduced to 0.18mV. When the atrial lead was sensing appropriately, the ventricular spike occurred after an appropriate AV delay, and this resulted in ventricular capture (Fig. 2B). The patient was evaluated by using fluoroscopy, which revealed that the ventricular lead was at the correct location, although the atrial lead was in close proximity to the tricuspid valve (Fig. 3). Therefore, it appeared that the atrial lead induced ventricular capture owing to its location, and this ventricular capture was sensed by the ventricular lead, causing the pacemaker to enter the safety pacing mode. This resulted in the second spike, which came in the refractory period, and did not capture the ventricle. Eventually, the atrial lead began sensing P waves, while pacing the ventricle. This diagnosis was confirmed by using the pacemaker׳s AOO mode, whereby atrial stimulation resulted in ventricular capture (Fig. 2C). Ventricular capture resulted in ventricular pacing by using a pacing threshold of 0.5V at 0.5ms pulse width. The lack of atrial detection was resolved by programming the highest device atrial sensing parameter (0.18mV), and the mode of the pacemaker was changed from DDD to VDD (Fig. 1B).